Activation of the renin-angiotensin-system has been associated with an increased risk of ischemic cardiovascular events independent of effects on blood pressure, while interruption of the renin-angiotensin-system by ACE inhibition reduced cardiovascular mortality in patients with left ventricular dysfunction. The mechanisms underlying these effects are not knows. One possible explanation involves an interaction between the RAS and fibrinolytic system. For example, Ang II stimulates expression of plasminogen activator inhibitor-1 in cultured endothelial cells in a dose-dependent manner. PAI-1 is the major physiologic inhibitor of fibrinolysis in vivo. In addition, by preventing the activation of matrix metalloproteinases by plasmin, PAI-1 may promote fibrosis. Increased PAI-1 expression is observed in atherosclerotic plazue and plasma PAI-1 is increased in patients with myocardial infarction.